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Reactive oxygen metabolite scavengers decrease functional coronary microvascular injury due to ischemia-reperfusion.

I M Dauber¹, E J Lesnefsky, K M VanBenthuysen

¹Division of Cardiology, Veterans Administration Medical Center, Denver 80220.

The American Journal of Physiology

|January 1, 1991

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Reactive oxygen metabolites contribute to coronary microvascular injury during ischemia-reperfusion. Superoxide dismutase (SOD) and dimethylthiourea (DMTU) significantly reduced microvascular permeability and protein leak in canine models.

Area of Science:

Cardiovascular Physiology
Microcirculation Research
Oxidative Stress Mechanisms

Background:

The precise role of reactive oxygen metabolites in ischemia-reperfusion coronary microvascular injury remains incompletely understood.
Investigating the impact of antioxidants on microvascular dysfunction following cardiac ischemia is crucial for therapeutic development.

Purpose of the Study:

To evaluate the efficacy of reactive oxygen metabolite scavengers, specifically superoxide dismutase (SOD) and dimethylthiourea (DMTU), in mitigating ischemia-reperfusion-induced coronary microvascular dysfunction.
To quantify the effect of SOD and DMTU on microvascular permeability using a protein leak index (PLI) in a canine model.

Main Methods:

Anesthetized dogs underwent 60 minutes of left anterior descending (LAD) coronary artery occlusion followed by 60 minutes of reperfusion.

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Animals were treated with either bovine superoxide dismutase (SOD), dimethylthiourea (DMTU), or saline (control).

Microvascular permeability was assessed using a double radioisotope protein leak index (PLI) method with radiolabeled autologous protein and red blood cells.

Main Results:

Ischemia-reperfusion significantly increased the protein leak index (PLI) in ischemic myocardium by over threefold compared to non-ischemic myocardium.
Superoxide dismutase (SOD) treatment reduced the ischemic PLI by 45%, while dimethylthiourea (DMTU) reduced it by 66%.
Both SOD and DMTU effectively reduced protein leak across all levels of regional ischemic blood flow without altering myocardial blood flow to the occluded LAD zone.

Conclusions:

Reactive oxygen metabolites play a significant role in ischemia-reperfusion-induced coronary microvascular injury.
Superoxide dismutase (SOD) and dimethylthiourea (DMTU) are effective in reducing microvascular permeability and protein leakage during cardiac ischemia-reperfusion.
These findings support the potential therapeutic benefit of antioxidant strategies in managing myocardial ischemia-reperfusion injury.